ArticleCerebellum (London, England)2012
Controlling Ca2+-activated K+ channels with models of Ca2+ buffering in Purkinje cells.
Article in Cerebellum (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Integrating physical units into high-performance AI-driven scientific computing.Nature communications · 2025Article
- Electrophysiological classification ofFrontiers in pharmacology · 2025Article
- Branch-specific clustered parallel fiber input controls dendritic computation in Purkinje cells.iScience · 2024Article
- Purkinje cell models: past, present and future.Frontiers in computational neuroscience · 2024Review
- Small-conductance calcium-activated potassium channels in the heart: expression, regulation and pathological implications.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Can neuron modeling constrained by ultrafast imaging data extract the native function of ion channels?Frontiers in computational neuroscience · 2023Article
- Modeling Neurons in 3D at the Nanoscale.Advances in experimental medicine and biology · 2022Article
- Computational models of neurotransmission at cerebellar synapses unveil the impact on network computation.Frontiers in computational neuroscience · 2022Review
- Influence of T-Bar on Calcium Concentration Impacting Release Probability.Frontiers in computational neuroscience · 2022Article
- Is Purkinje Neuron Hyperpolarisation Important for Cerebellar Synaptic Plasticity? A Retrospective and Prospective Analysis.Cerebellum (London, England) · 2020Review
- Cerebellar Golgi cell models predict dendritic processing and mechanisms of synaptic plasticity.PLoS computational biology · 2020Article
- Two Distinct Sets of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Calcium-activated SK channels control firing regularity by modulating sodium channel availability in midbrain dopamine neurons.Scientific reports · 2017Article
- Concise Whole-Cell Modeling of BKBiophysical journal · 2017Article
- Impact of calcium-activated potassium channels on NMDA spikes in cortical layer 5 pyramidal neurons.Journal of neurophysiology · 2016Article
- Calcium regulation of HCN channels supports persistent activity in a multiscale model of neocortex.Neuroscience · 2016Article
- Multitarget Multiscale Simulation for Pharmacological Treatment of Dystonia in Motor Cortex.Frontiers in pharmacology · 2016Article
- Calcium-Activated Potassium Channels at Nodes of Ranvier Secure Axonal Spike Propagation.Cell reports · 2015Article
- Modeling auditory coding: from sound to spikes.Cell and tissue research · 2015Review
- Duration of Purkinje cell complex spikes increases with their firing frequency.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular Ca(2+) concentrations play a crucial role in the physiological interaction between Ca(2+) channels and Ca(2+)-activated K(+) channels. The commonly used model, a Ca(2+) pool with a short relaxation time, fails to simulate interactions occurring at multiple time scales. On the other hand, detailed computational models including various Ca(2+) buffers and pumps can result in large computational cost due to radial diffusion in large compartments, which may be undesirable when simulating morphologically detailed Purkinje cell models. We present a method using a compensating mechanism to replace radial diffusion and compared the dynamics of different Ca(2+) buffering models during generation of a dendritic Ca(2+) spike in a single compartment model of a PC dendritic segment with Ca(2+) channels of P- and T-type and Ca(2+)-activated K(+) channels of BK- and SK-type. The Ca(2+) dynamics models used are (1) a single Ca(2+) pool; (2) two Ca(2+) pools, respectively, for the fast and slow transients; (3) detailed Ca(2+) dynamics with buffers, pump, and diffusion; and (4) detailed Ca(2+) dynamics with buffers, pump, and diffusion compensation. Our results show that detailed Ca(2+) dynamics models have significantly better control over Ca(2+)-activated K(+) channels and lead to physiologically more realistic simulations of Ca(2+) spikes and bursting. Furthermore, the compensating mechanism largely eliminates the effect of removing diffusion from the model on Ca(2+) dynamics over multiple time scales.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.